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Biomedical subjects

J Shani

Publications and source records attributed to J Shani.

At least 127 records · Page 7Linked to original sources
PubMed1981

Effect of androstanediol sulfates on luteinizing hormone release in ovariectomized rats.

Androstanediols are the major products of the immature rat ovary and are present in peripheral circulation mainly as sulfate conjugates. In this paper we identified 5 alpha-androstane-3 beta, 17 beta-diol-3-monosulfate (3 beta-A-MS) as one of the forms found in blood and subsequently synthesized and administered it to ovariectomized rats at a dose of 100 microgram/100 g BW . day from 21-45 days of age. This dose effectively inhibits postcastrational LH elevation. Other androstanediols examined, like 5 alpha-A-3 alpha, 17 beta-diol-disulfate, 5 alpha-A-3 beta, 17 beta-diol-disulfate, and the free 5 alpha-A-3 beta, 17 beta-diol do not exert such an effect on LH release. The MCR of 3 beta-A-MS was 441 +/- 64 ml/h, independent of the infusion rate between 0.15-15.0 microgram/h, and its production rate was calculated to be 37 microgram/day at the age of 30 days. The quantitative relations of the steroid level in serum to its capacity to inhibit LH release was studied using Silastic capsules. A steady concentration of 1.1 ng 3 beta-A-MS/ml serum inhibits postcastrational LH release in the immature female rat. Since a similar or higher concentration of the steroid is present in the intact rat, it is assumed that 3 beta-A-MS controls pituitary LH release in the intact immature female rat. (Endocrinology 108: 500, 1981)

Androstane-3,17-diol↗
PubMed1980

Range-related glycaemic response to increasing load of carbohydrates.

The glycaemic response to feeding increased loads of glucose and sucrose was investigated in man and rat. Assessed were the tolerance tests after feeding 10-100 g glucose or 10-20 g sucrose to hospitalized diabetic or non-diabetic patients and after loading 30-450 mg glucose or sucrose per 100 g body weight to alloxan-diabetic or non-diabetic rats. The maximal levels of tolerance curves, the increase in blood glucose levels and the sum of the glycaemic values reflecting the areas under the curves were chosen as criteria. The correlation between the dose of ingested carbohydrates and the glyucaemic effect was not necessarily linear, but blood glucose values following the carbohydrate loads were concentrated in ranges, corresponding to groups of load sizes. These observations may be practical for the diagnostic procedure and dietetic treatment of the diabetic patient.

Aged↗
PubMed1980

Demonstration of prolactin-releasing activity in the pigeon.

The capacity of the pigeon pituitary gland to release prolactin was investigated in vivo, to evaluate its hypothalamic regulation and to establish the dominant hypothalamic factor for prolactin secretion. After 3 days of systemic administration of some physiological and pharmacological agents, followed by 2 consecutive days of local intradermal injections of prolactin into their crop sacs, the crop mucosa was scraped, dried and weighed. The substances tested were: oestradiol and tamoxifen (antioestrogen), thyrotophin-releasing hormone (TRH) and anti-TRH serum, perphenazine (releases prolactin in mammals) and bromocriptine (suppresses prolactin in mammals). Prolactin and anti-prolactin serum were tested as controls. While prolactin markedly proliferated and anti-prolactin serum significantly inhibited the mucosal weight, oestradiol, TRH and perphenazine dramatically depressed proliferation of the mucosa, suggesting that prolactin secretion was inhibited. Tamoxifen, anti-TRH serum and bromocriptine significantly increased the proliferation of the crop mucosa, indicating an increase in the endogenous release of prolactin. Since the effect of these substances on prolactin release in the pigeon is the opposite from their well-established effects in mammals, these results suggest, in a specific and homologous model, that the dominating regulator for prolactin in the pigeon is contrary to that in the mammal, namely prolactin-releasing factor, and that TRH may play a significant role in the physiological regulation of prolactin secretion.

Animals↗
PubMed1979

Enkephalin levels in rat brain after various regimens of morphine administration.

Rats implanted with a single morphine pellet for a short period of 72 h have been shown to have a lower concentration of enkephalin in the brain, as determined by a radioimmunoassay (RIA) detecting Leu- and Met-enkephalin as well as another endogenous substance. Two other paradigms of morphine implantations did not cause any change in enkephalin levels. Various protocols of morphine injections failed to elicit changes in enkephalin content in the rat brain. The significant decrease observed after the short regimen implantation suggests that at a certain stage in the development of physical dependence a reduction in the amount of enkephalin occurs, but returns to normal values within a short period.

Animals↗
PubMed1979

Pinealectomy-induced changes in blood and pituitary luteinizing and prolactin levels during the last phase of pregnancy in rats.

Serum LH levels were higher in pinealectomized than in sham-operated control rats during all 4 of the last days of pregnancy studied, although reaching significance only during the final 2 days, 21 and 22. Prolactin (Prl) levels in the serum on the final day of pregnancy, and its contents in the pituitary throughout the entire study period, were significantly lower in pinealectomized rats. Pituitary weights were lower in pinealectomized than in control animals during days 21 and 22 of pregnancy, but no differences were found between the 2 groups in the average number of living foetuses and resorptions. The results presented would seem to indicate that during the last phase of pregnancy the pineal gland plays a role in the modification of gonadotropin synthesis and release. It appears that with LH the release, and with Prl mainly the synthesis, is being affected by the pineal, although the release of Prl may be influenced as well.

Animals↗
PubMed1979

Characterization of the specific binding of prolactin to binding sites in the seminal vesicle of the rat.

The binding of ovine prolactin to the seminal vesicles of the rat has been characterized and found to be a saturable process, dependent upon time, temperature, protein concentration of the seminal vesicle and divalent ions. Its specificity was similar to that reported for prolactin binding to other organ preparations. Time and temperature studies of the specific binding revealed that equilibrium was reached after 16 h at 5 degrees C or 4 h at 19 degrees C. Nonspecific binding was also dependent on time and temperature. This parameter has been reported to comprise up to 70% of the total binding to various organ-binding sites, but it fell to below 20% after 48 h at 19 degrees C, thus demonstrating the high degree of specificity required of target organ receptors. From degradation studies it was evident that no damage occurred to the free hormone during incubation for up to 70 h at 5 degrees C or 16 h at 19 degrees C. However, there seems to be a difference in the susceptibility of bound and free ovine prolactin to damage during incubation: after 40 h at 19 degrees C the hormone in the supernatant fraction had lost 85% of its binding ability, whereas a high level of specific binding was evident in the pellet. A Scatchard plot of competitive binding studies revealed two classes of binding sites, of which the high-affinity, low-capacity site was similar to that reported previously and consistent with a physiological receptor for prolactin in the seminal vesicle of the rat.

Animals↗
PubMed1979

Effect of the timing of perphenazine administration on pregnancy in the rat.

Perphenazine in doses of 10--50 mg kg-1 day-1 given at the early stages of pregnancy delayed nidation up to day 8 of pregnancy. Once nidation had occurred the length of the rest of the gestation period was normal. Doses of up to 20 mg perphenazine kg-1 day-1, injected on days 1--7, prolonged gestation but the mothers and young were apparently normal; lower doses were effective only when treatment commenced soon after copulation. The delay in implantation of the ovum caused by perphenazine was corrected and and implantation was brought about immediately, by injection of 0.1 microgram oestradiol together with perphenazine. It is suggested that perphenazine delays and prevents implantation in rats by counteracting oestrogen release from the ovaries.

Animals↗
PubMed1978

Reciprocal effects of prolactin and thyroxine on the growth rate of rat pups from weaning to puberty.

Prolactin and thyroxine were added to the daily diet of rat pups from weaning to puberty (days 20--40). While prolactin significantly retarted the pups' growth, thyroxine stimulated growth and even compensated for the depression caused by prolactin. The significant retardation in the growth of the prolactin-treated pups around days 30--35 of age indicates that at that period they are extremely prolactin-dependent, thus confirming previous reports that exogenous prolactin inhibits its own endogenous secretion. On the other hand, the possible growth promotion caused by thyroxine is mild and does not initiate a feedback mechanism. This suggests that prolactin is indispensable for the normal development of the weaned, immature rat.

Animals↗
PubMed1977

Suppression of prolactin and thyrotropin secretion in the rat by antiserum to thyrotropin-releasing hormone.

Administration of antiserum to synthetic thyrotropin-releasing hormone (TRH) to male and female rats cause a 50% and a 70% suppression in serum levels of prolactin and thyrotropin, respectively, as compared with controls injected with normal rabbit serum. The degree of suppression was similar in diestrous and proestrous female rats and in male rats. These findings support the view that, in addition to its original designation, TRH also has a physiological role in regulating release of pituitary prolactin.

Animals↗
PubMed1977

Effect of thyrotrophin-releasing hormone on serum prolactin levels in men with azoospermia.

Infertile men with azoospermia and low testosterone levels because of Klinefelter's or Sertoli cell-only syndrome responded to a single injection of TRH by an increase in serum prolactin levels. The degree of this response was not as great as in fertile men with normospermia and normal testosterone levels, although initial prolactin levels had been similar in both groups. The results demonstrate a link between testosterone and prolactin levels in fertile and infertile men.

Humans↗